Vulnerability to sympathetic stress does not persist in takotsubo stress cardiomyopathy.

OBJECTIVE: Our objective was to investigate whether dobutamine stress echocardiography (DSE) could induce abnormal cardiac function in takotsubo stress cardiomyopathy (TSC) patients in a stable condition after the acute attack. METHODS AND RESULTS: This was a case-control study and a substudy of the Stockholm Myocardial Infarction With Normal Coronaries (SMINC) study. Twenty-two patients with a previous episode of TSC and 22 sex- and age-matched control subjects were recruited from the SMINC study and investigated with the use of DSE. All TSC patients had a previous normal cardiovascular magnetic resonance investigation. Tissue Doppler imaging-derived time phases of the cardiac cycle were recorded to calculate myocardial performance index (MPI) to assess ventricular function. Compared with control subjects at rest, TSC patients had a slightly but significantly higher left ventricular MPI (LV-MPI; 0.53 vs 0.59; P = .01) and as a trend higher right ventricular MPI (0.38 vs 0.47; P = .08), although during DSE these variables did not differ significantly. CONCLUSION: We found no difference in standard diastolic parameters between TSC and control subjects, but a significant higher value in LV-MPI in the TSC group at rest. However, no such difference could be demonstrated during DSE between the groups, indicating that vulnerability to sympathetic stimulation does not persist in TSC patients.

Corrigendum: Effects on Subclinical Heart Failure in Type 2 Diabetic Subjects on Liraglutide Treatment vs. Glimepiride Both in Combination with Metformin: A Randomized Open Parallel-Group Study.

[This corrects the article on p. 325 in vol. 8, PMID: 29184539.].

Effects on Subclinical Heart Failure in Type 2 Diabetic Subjects on Liraglutide Treatment vs. Glimepiride Both in Combination with Metformin: A Randomized Open Parallel-Group Study.

Objective: We aimed to investigate the effect of liraglutide treatment on heart function in type 2 diabetes (T2D) patients with subclinical heart failure. Methods: Randomized open parallel-group trial. 62 T2D patients (45 male) with subclinical heart failure were randomized to either once daily liraglutide 1.8 mg, or glimepiride 4 mg, both add on to metformin 1 g twice a day. Mitral annular systolic (s') and early diastolic (e') velocities were measured at rest and during bicycle ergometer exercise, using tissue Doppler echocardiography. The primary endpoint was 18-week treatment changes in longitudinal functional reserve index (LFRIdiastolic/systolic). Results: Clinical characteristics between groups (liraglutide = 33 vs. glimepiride = 29) were well matched. At baseline left ventricle ejection fraction (53.7 vs. 53.6%) and global longitudinal strain (-15.3 vs. -16.5%) did not differ between groups. There were no significant differences in mitral flow velocities between groups. For the primary endpoint, there was no treatment change [95% confidence interval] for: LFRIdiastolic (-0.18 vs. -0.53 [-0.28, 2.59; p = 0.19]), or LFRIsystolic (-0.10 vs. -0.18 [-1.0, 1.7; p = 0.54]); for the secondary endpoints, there was a significant treatment change in respect of body weight (-3.7 vs. -0.2 kg [-5.5, -1.4; p = 0.001]), waist circumference (-3.1 vs. -0.8 cm [-4.2, -0.4; p = 0.019]), and heart rate (HR) (6.3 vs. -2.3 bpm [-3.0, 14.2; p = 0.003]), with no such treatment change in hemoglobin A1c levels (-11.0 vs. -9.2 mmol/mol [-7.0, 2.6; p = 0.37]), between groups. Conclusion: 18-week treatment of liraglutide compared with glimepiride did not improve LFRIdiastolic/systolic, but however increased HR. There was a significant treatment change in body weight reduction in favor for liraglutide treatment.

Assessment of left ventricular function using mitral annular velocities in patients with congestive heart failure with or without the presence of significant mitral regurgitation.

Myocardial velocities in patients with congestive heart failure (CHF) were studied using pulsed wave Doppler tissue imaging. Velocities were recorded at the mitral and tricuspid annulus. Four sites at the mitral annuli were selected corresponding to the septal, lateral, inferior, and anterior walls of the left ventricle from apical 4- and 2-chamber views. A mean value from the above 4 sites was selected to describe the mitral annular velocities. Only one site of the tricuspid annulus was selected, corresponding to the right ventricular free wall. Three different annular velocities were recorded: the peak systolic, and the peak early and late diastolic velocities. A total of 96 patients were compared with 12 age-matched healthy participants. Patients with CHF had significantly decreased mitral and tricuspid systolic velocities compared with healthy participants (4.9 vs 9.3 cm/s, P <.001, for the mitral annulus and 10.4 vs 14.6 cm/s, P <.001, for the tricuspid annulus). The early diastolic velocity was also reduced in patients compared with healthy participants (5.9 vs 10.9 cm/s, P <.001, for the mitral annulus and 8.6 vs 12.9 cm/s, P <.001, for the tricuspid annulus). Patients with CHF had a severely depressed left ventricular ejection fraction (EF) (27%). The correlation the between systolic mitral annular velocity and EF was relatively good (r = 0.59 and P <.001). The patients with CHF were divided into 2 subgroups depending on the presence or absence of significant mitral regurgitation. There was a correlation between EF and the systolic mitral annular velocity both in patients with (r = 0.61, P <.001) and without (r = 0.59, P <.001) significant mitral regurgitation. In conclusion, compared with healthy participants, the mitral and tricuspid annular velocities are significantly decreased in patients with CHF. The correlation between EF and the systolic mitral annular velocity is relatively good irrespective of the presence or absence of significant mitral regurgitation. Measurements of annular velocities constitute a simple and useful method for evaluating patients with CHF.

Acute effects of smoking on diastolic function in healthy participants: studies by conventional doppler echocardiography and doppler tissue imaging.

The acute effects of smoking on left ventricular (LV) function were studied in 36 healthy participants (mean age 38 +/- 10 years). The studies were made before and immediately and 30 minutes after smoking a cigarette. From apical 4- and 2-chamber views, the mitral annular velocities, determined by pulsed wave Doppler tissue imaging, were measured at 4 LV sites corresponding to the septum and the anterior, lateral, and inferior walls. A mean value from the 4 sites was used to assess LV function. The peak systolic, early diastolic, late diastolic, and the ratio of early to late diastolic velocities were recorded. In addition, other conventional Doppler echocardiographic diastolic parameters were also determined. Heart rate was increased immediately after smoking (from 67 +/- 8 to 74 +/- 10 bpm, P <.001). There was no change in systolic mitral annular velocity. Diastolic LV function was changed significantly immediately after smoking. The transmitral A wave increased (0.55 +/- 0.1 vs 0.7 +/- 0.1 m/s, P <.001), the transmitral E/A ratio decreased (1.5 +/- 0.6 vs 1.1 +/- 0.3, P <.001), and the transmitral E-wave deceleration time increased (186 +/- 42 vs 211 +/- 44 ms, P <.05). The diastolic myocardial velocity at the mitral annulus also changed significantly: the early diastolic velocity decreased (16 +/- 3 vs 15 +/- 3 cm/s, P <.001), the late diastolic velocity increased (10.9 +/- 2.2 vs 12 +/- 2.4 cm/s, P <.001), and the ratio of early to late diastolic annular velocities decreased (1.5 +/- 0.5 vs 1.2 +/- 0.4, P <.001). The changes in the transmitral flow velocities remained unaltered even 30 minutes afterward, although the heart rate returned to normal. The results were similar in both smokers and nonsmokers. Acute smoking of a cigarette influences LV diastolic function in healthy participants. The mechanism behind this effect cannot be explained only by changes in the heart rate or loading conditions. The mechanism is probably more complex.

Left Ventricular Regional Diastolic Dysfunction in Patients with First Myocardial Infarction Determined by Diastolic Motion of the Atrioventricular Plane.

Motion of the left ventricular [left ventricle (LV)] atrioventricular (AV) plane has been used to assess systolic LV function. The method has not been used properly to assess diastolic function, especially after a first myocardial infarction (MI). The diastolic function was assessed in 47 previously healthy patients with a first MI assessed by echocardiographic diastolic motion of the LV AV plane. The motion of the AV plane was recorded at four different LV sites, that is, at the septal, anterior, lateral, and inferior walls. Two distinct phases of motion were noticed during diastole at all the sites: one at the early diastole caused by rapid filling of the LV and the other at late diastole during the atrial contraction. The contribution of left atrial contraction to LV filling at different LV sites was calculated by relating the magnitude of the motion caused by atrial contraction to the total diastolic AV plane motion at the respective sites. These left atrial contributions were regarded as the regional diastolic function of the respective LV sites. The global LV diastolic function was determined from the left atrial contribution to total AV plane motion from the above four sites. Patients with anterior MI had a significantly lower ejection fraction than those with inferior MI (41% and 49%, respectively; P < 0.01). Compared with age-matched healthy subjects, the regional atrial contribution to diastolic filling was significantly higher at the anterior wall in anterior MI (38% and 52%, respectively; P < 0.001) and at the inferior wall in inferior MI (43% and 53%, respectively; P < 0.01). The atrial contribution to global LV filling was increased in anterior MI (48% compared with 42% in healthy subjects; P < 0.05) but not in inferior MI. These findings suggest that the diastolic AV plane displacement (AVPD) may be used to assess both the regional and the global diastolic function in patients following an MI.